Weil-Fugazza J, Godefroy F, Besson J M
Brain Res. 1979 Oct 19;175(2):291-301. doi: 10.1016/0006-8993(79)91008-4.
The effects of morphine (10 mg/kg/s.c.) on tryptophan (TRP), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels were studied in normal and arthritic rats. (1) In normal rats morphine induced a discrete but significant increase of 5-HIAA levels in the forebrain and the spinal cord. (2) By contrast, in rats suffering from experimentally induced arthritis large modifications were apparent. The basal levels of TRP, 5-HT and 5-HIAA were significantly higher than in normal rats. Morphine induced clear increases of 5-HIAA and TRP in the forebrain, the brain stem and the spinal cord, without any modification of 5-HT. The effects were dose-dependent and suppressed by naloxone (1 mg/kg/i.m.). Statistical analysis clearly revealed that arthritic rats were much more sensitive to morphine. The results support the hypothesis of an activation of a 5-HT descending pathway by morphine which parallels the activation of the ascending pathway previously demonstrated by several authors and confirmed here.
研究了吗啡(10毫克/千克/皮下注射)对正常大鼠和关节炎大鼠体内色氨酸(TRP)、5-羟色胺(5-HT)及5-羟吲哚乙酸(5-HIAA)水平的影响。(1)在正常大鼠中,吗啡致使前脑和脊髓中5-HIAA水平出现离散但显著的升高。(2)相比之下,在实验性诱导关节炎的大鼠中,明显出现了大幅变化。TRP、5-HT和5-HIAA的基础水平显著高于正常大鼠。吗啡使前脑、脑干和脊髓中的5-HIAA和TRP明显升高,而5-HT无任何变化。这些效应呈剂量依赖性且被纳洛酮(1毫克/千克/肌肉注射)抑制。统计分析清楚地显示,关节炎大鼠对吗啡更为敏感。结果支持了吗啡激活5-羟色胺下行通路的假说,这与先前几位作者所证实并在此得到确认的吗啡激活上行通路相平行。